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Cells
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Animal Models for the Research of Alzheimer's Disease and Neurodegeneration
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Animal Models for the Research of Alzheimer's Disease and Neurodegeneration

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Aging".

Deadline for manuscript submissions: closed (16 August 2023) | Viewed by 1323

Special Issue Editors

Dr. Dongming Cai

E-Mail Website
Guest Editor
Department of Neurology, Icahn School of Medicine at Mount Sinai, 1468 Madison Avenue, New York, NY 10029, USA
Interests: phospholipids; Alzheimer's disease; mouse models; apolipoprotein; endo-lysosomal pathways; drug development
Special Issues, Collections and Topics in MDPI journals
Dr. Mariana Lemos Duarte

E-Mail Website
Guest Editor
MSSM Department of Neurology, Icahn School of Medicine at Mount Sinai, 1468 Madison Avenue, New York, NY 10029, USA
Interests: Alzheimer's disease; memory; mouse models; human-induced pluripotent stem cells; phospholipids; kinase signaling; molecular pharmacology; tauopathy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Alzheimer’s disease (AD) is a major healthcare burden with a large patient population. Currently there are no effective therapies to stop or slow down the progression of AD. The major challenge in this field is the lack of a better understanding of AD pathophysiology due to its multifaceted disease mechanisms. Animal models have been widely utilized in AD research to study the pathogenesis of AD and test drug efficacy at pre-clinical stages. In the past decade or so, innovative approaches have been developed including novel animal modeling technologies to better recapitulate pathological changes in AD and neurodegeneration in vivo, and to guide the preclinical development of efficacious therapies for AD.

This Special Issue will examine the currently available mouse models of AD, including both familial and sporadic AD mouse models, as well as other animal models. The development of animal models of AD-related neurodegenerative disorders will be explored as well. The pathological and behavioral phenotypes of various animal models of AD and neurodegenerative disorders will be discussed. The approaches of modeling environmental and genetic risk factors of AD in vivo in animals, as well as the selection of animal modeling for preclinical drug development in AD, will be investigated. 

You may choose our Joint Special Issue in Geriatrics.

Dr. Dongming Cai
Dr. Mariana Lemos Duarte
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Alzheimer’s disease (AD)
  • animal models
  • disease mechanisms
  • pathological changes
  • behavioral phenotypes
  • environmental factors
  • genetic risk factors
  • drug development

Published Papers (1 paper)

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Research

21 pages, 5102 KiB  
Article
Alzheimer’s Disease-like Pathological Features in the Dorsal Hippocampus of Wild-Type Rats Subjected to Methionine-Diet-Evoked Mild Hyperhomocysteinaemia
by Maria Kovalska, Petra Hnilicova, Dagmar Kalenska, Marian Adamkov, Libusa Kovalska and Jan Lehotsky
Cells 2023, 12(16), 2087; https://doi.org/10.3390/cells12162087 - 17 Aug 2023
Cited by 1 | Viewed by 1073
Abstract
Multifactorial interactions, including nutritional state, likely participate in neurodegeneration’s pathogenesis and evolution. Dysregulation in methionine (Met) metabolism could lead to the development of hyperhomocysteinaemia (hHcy), playing an important role in neuronal dysfunction, which could potentially lead to the development of Alzheimer’s disease (AD)-like [...] Read more.
Multifactorial interactions, including nutritional state, likely participate in neurodegeneration’s pathogenesis and evolution. Dysregulation in methionine (Met) metabolism could lead to the development of hyperhomocysteinaemia (hHcy), playing an important role in neuronal dysfunction, which could potentially lead to the development of Alzheimer’s disease (AD)-like pathological features. This study combines proton magnetic resonance spectroscopy (1H MRS) with immunohistochemical analysis to examine changes in the metabolic ratio and histomorphological alterations in the dorsal rat hippocampus (dentate gyrus—DG) subjected to a high Met diet. Male Wistar rats (420–480 g) underwent hHcy evoked by a Met-enriched diet (2 g/kg of weight/day) lasting four weeks. Changes in the metabolic ratio profile and significant histomorphological alterations have been found in the DG of hHcy rats. We have detected increased morphologically changed neurons and glial cells with increased neurogenic markers and apolipoprotein E positivity parallel with a diminished immunosignal for the N-Methyl-D-Aspartate receptor 1 in hHcy animals. A Met diet induced hHcy, likely via direct Hcy neurotoxicity, an interference with one carbon unit metabolism, and/or epigenetic regulation. These conditions lead to the progression of neurodegeneration and the promotion of AD-like pathological features in the less vulnerable hippocampal DG, which presents a plausible therapeutic target. Full article
(This article belongs to the Special Issue Animal Models for the Research of Alzheimer's Disease and Neurodegeneration)
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